Background & Aims In the normal liver, hepatocytes form a uniquely polarised cell layer that
enables movement of solutes from sinusoidal blood to canalicular bile. Whilst several
cholestatic liver diseases with defects of hepatocyte polarity have been identified, the
molecular mechanisms of pathogenesis are not well defined. One example is
arthrogryposis, renal dysfunction and cholestasis syndrome, which in most patients is
caused by VPS33B mutations. VPS33B is a protein involved in membrane trafficking that …